The present invention generally relates to treating cartilage defects. More specifically, the present invention relates to a method for treating cartilage defects, for example osteoarthritis, rheumatoid arthritis, and cartilage injuries, by moving ions into a collagen matrix of the defective cartilage using electricity.
Human joint surfaces are covered by articular cartilage, a low friction, durable material that distributes mechanical forces and protects the underlying bone. Injuries to articular cartilage are common, especially in the knee. Data from the Center for Disease Control (CDC) and clinical studies have suggested that approximately 100,000 articular cartilage injuries occur per year in the United States. Such injuries occur most commonly in young active people and result in pain, swelling, and loss of joint motion. Damaged articular cartilage does not heal. Typically, degeneration of the surrounding uninjured cartilage occurs over time resulting in chronic pain and disability. Cartilage injuries therefore frequently lead to significant loss of productive work years and have enormous impact on patients' recreation and lifestyle.
Generally, there are three main types of cartilage: hyaline cartilage, elastic cartilage, and fibrocartilage. Hyaline cartilage is the most abundant type of cartilage. Hyaline cartilage lines the bones in articular joints and also serves as a center of ossification. Elastic cartilage mainly provides support and elasticity, for example, in the pinna of the ear or in the larynx. It is similar to articular cartilage but contains elastin throughout the matrix. Fibrocartilage is found in the areas that require tough support or tensile strength, for example in the pubic area. It has more collagen than the other types of cartilage which gives it strength. Fibrocartilage replaces hyaline cartilage or articular cartilage in osteoarthritis.
Hyaline cartilage or articular cartilage is mainly the important architectural form of the tissue, which has multiple zones. Each zone, such as a superficial, middle and deep zone, has a role in the physiology of the cartilage. In the superficial zone, the collagen fibers run parallel to the surface. The superficial zone is most exposed to loading and has the highest tensile property.
Articular cartilage has four main components: collagen fibers, chondrocytes, water, and proteoglycans. Collagen fibers are responsible for the form and tensile properties of the tissue. Chondrocytes maintain the matrix. Water is about 80% by wet weight (FCD) in the tissue. Water content is governed by the FCD (Fixed Charged Density) of proteoglycans. A high concentration of proteoglycans, predominantly aggrecans, is responsible for the osmotic swelling that exerts on the collagen network. It is the retention of aggrecan in compressed form within the collagen network that causes the swelling pressure and makes cartilage ideal for resisting compressive loads, thereby supporting its function as a tough and resilient load-bearing surface.
The stiffness of cartilage is determined by the interaction of the three phases of cartilage: collagen fibers, proteoglycans, and the water. In other words, the load-bearing of cartilage is provided by the tensile properties of the collagen fibers and osmotic swelling pressure of aggrecan.
Referring to FIGS. 1A-1B, osteoarthritis is where cartilage degeneration is associated with loss of structural and functional integrity. For comparison, FIG. 1A shows a normal joint and an osteoarthritic joint (FIG. 1B) with a breakdown of cartilage. Osteoarthritis is not an inflammatory disease but it becomes inflamed after several pieces of cartilage are freed from the tissue inside the synovial fluid. Early swelling of cartilage leads through the dilution of proteoglycans, mainly aggrecans, out of the tissue to increased hydraulic permeability and decreased osmotic pressure. Increased hydraulic permeability means that water starts to flow into cartilage where it is not retained by the aggrecan since they are diluted in the synovial fluid. Afterwards, the collagen matrix starts to break down and deteriorate.
Currently, there are many treatments for the symptoms of osteoarthritis including: exercise, weight control, stress relief, drugs, surgery, and biologics. Biologics are a more recent treatment that includes autologous chondrocyte implantation, sterile artificial matrices, and hyaluronan.
However, non-steroidal anti-inflammatory drugs (NSAIDs) remain the primary treatment modality for osteoarthritis. It is unknown whether the efficacy of NSAIDs is dependent upon their analgesic or anti-inflammatory properties or the slowing of degenerative processes in the cartilage. There is also a concern that NSAIDs may be deleterious to patients. For example, NSAIDs have well known toxic effects in the stomach, gastrointestinal tract, liver and kidney. However, aspirin inhibits proteoglycan synthesis and normal cartilaginous repair processes in animals. One study in humans suggested that indomethacin might accelerate breakdown of hip cartilage. All adverse effects appear more commonly in the elderly—the very population most susceptible to osteoarthritis.
Therefore, there remains a need for an effective treatment of cartilage defects. There is a need for a method of replacing the proteoglycans missing in a collagen matrix due to cartilage defects. There is also a need for a method for treating cartilage defects that maintains the balance between the three phases of cartilage. Also, there is a further need for a method of treating cartilage defects without any adverse side effects and minimal invasive surgery. Finally, there is a need to provide a method for treating cartilage defects which controls pain, improves joint function, maintains normal body weight, and achieves a health lifestyle.